Built from the Selank, Semax research profiles · Profiles last updated October 1, 2026 · Reviewed by The Peptide Dispatch Editorial Team
This page compares Selank and Semax using only their research-profile data. Selank (research stage: Approved outside US; half-life: Not established in published research). It is a lab-made peptide thought to act on the brain's calming (GABA) system, based mostly on animal studies. Semax (research stage: Approved outside US; half-life: Not established in published research). It is a peptide studied mainly in rats after stroke, where it changed the activity of inflammation- and nerve-related genes. Educational summary, not medical advice.
Where each point comes from: Clinicalhuman trials and FDA labels Lab / animalrodent, cell and ex vivo studies Community-reporteduser experience and commonly used protocols, not from clinical studies
| Selank | Semax | |
|---|---|---|
| Category | Cognitive | Cognitive |
| Research status | Approved outside US | Approved outside US |
| Regulatory note (as of Sept 2026) | Not FDA-approved; not among the six peptides PCAC recommended for the 503A Bulks List in July 2026. Regulatory tracker → | Not FDA-approved. Removed from 503A Category 2 on April 15, 2026. PCAC recommended for the 503A Bulks List (advisory); awaiting FDA rulemaking; not lawfully compoundable under 503A as of Sept 17, 2026. PCAC vote: 8–5–1 (yes–no–abstain), July 24, 2026. Regulatory tracker → |
| Half-life | No published PK data found | No published PK data found |
| Administration route | Intranasal | Intranasal |
| Dosing used in published research (not a recommendation) | 0.3 mg/kg i.p. (anxiolytic dose) in rats and mice; single injection in healthy human volunteers in an fMRI study (n=52, dose not in abstract) | 6000 micrograms/day intranasally for 10 days, repeated after a 20-day interval, in a clinical study of 110 post-ischaemic-stroke patients; rodent neuroprotection work uses the transient middle cerebral artery occlusion model in rats |
| Community-reported protocol (not from clinical studies) | Community-reported250–500 mcg, intranasal | Community-reported200–600 mcg, intranasal |
| How it works (as summarized from the cited research) | In plain terms: It is a lab-made peptide thought to act on the brain's calming (GABA) system, based mostly on animal studies. Proposed mechanism, from animal studies and a review: a synthetic tuftsin analogue proposed to act on GABA-related systems (review, Doyno 2021). Anxiolytic-like effects were reported in rats (Kasian 2017); a human fMRI study (n=52 healthy volunteers) examined its effects on resting-state brain connectivity (Panikratova 2020). | In plain terms: It is a peptide studied mainly in rats after stroke, where it changed the activity of inflammation- and nerve-related genes. Proposed mechanism, from rodent studies: in a rat ischaemia-reperfusion stroke model, semax suppressed inflammatory gene expression and increased expression of neurotransmission-related genes (Filippenkov 2020). Claims that semax raises brain BDNF or modulates dopamine and serotonin come from rodent work, not human studies; in humans, a clinical study of 110 post-stroke patients reported higher plasma BDNF (Gusev 2018). |
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| Profile description | Synthetic analog of the immunomodulatory peptide tuftsin, with anxiolytic-like effects reported in rodent models and limited human data. Developed alongside Semax in Russia. | Synthetic peptide derived from ACTH, developed in Russia and approved there for stroke and cognitive disorders. In a clinical study of 110 post-stroke patients, semax raised plasma BDNF and accelerated functional recovery. |
| References cited on the profile | 4 | 2 |
For the sourced, dated status of every peptide in FDA's 2026 compounding actions, see the FDA peptide regulatory tracker.
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Educational content — not medical advice. Effects described are drawn from cited research in study subjects.